scholarly journals Near fatal stent thrombosis in an aneurysmatic RCX as first manifestation of heparin induced thrombocytopenia (HIT) without thrombocytopenia

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Marc Zoller ◽  
Iskandar Atmowihardjo ◽  
Jeanette Huch ◽  
Ines Albrecht ◽  
Dirk Habedank
Keyword(s):  
Stent Thrombosis ◽  
Thrombotic Event ◽  
Coronary Intervention ◽  
Clinical Event ◽  
Platelet Factor ◽  
Heparin Induced Thrombocytopenia ◽  
Case Presentation ◽  
Normal Platelet ◽  
Activation Assay ◽  
Acute Stent Thrombosis

Abstract Background Thrombosis resulting from heparin-induced thrombocytopenia (HIT) occurs in about 2% of patients without a significant decrease in platelet counts. We report on such a near fatal thrombotic event caused by coronary intervention. Case presentation A supposedly “completely healthy” 53-year-old patient was admitted to hospital with covered rupture of an aneurysm of the Aorta descendens. He was successfully operated on and underwent coronary angiography due to NSTEMI six days later. Immediately after intervention of a 90% RCX stenosis he developed ventricular flutter, was defibrillated, and re-angiography showed partial occlusion of the RCX stent. Lots of white thrombi could be retrieved by aspiration catheter and gave reason for a HIT without thrombocytopenia. The detection of platelet factor 4/heparin complex antibodies by immunoassay supported and the subsequent Heparin Induced Platelet Activation Assay proved this diagnosis. Conclusions The clinical event of an acute stent thrombosis should alarm the interventional team to the diagnosis of HIT even with a normal platelet count.

The Incidence of Thrombosis in Patients with Isolated Heparin Induced Thrombocytopenia.

Blood ◽  
2006 ◽  
Vol 108 (11) ◽  
pp. 1049-1049 ◽  
Author(s):  
Rachel P. Rosovsky ◽  
Omar I. Abdel-Wahad ◽  
Elizabeth M. Van Cott ◽  
David J. Kuter
Keyword(s):  
Platelet Count ◽  
Mortality Rate ◽  
Massachusetts General Hospital ◽  
Thrombotic Event ◽  
Radiographic Examination ◽  
Platelet Factor ◽  
Heparin Induced Thrombocytopenia ◽  
Total Incidence ◽  
Objective Evidence ◽  
Heparin Exposure

Abstract Introduction: Heparin-induced thrombocytopenia type-II (HIT) is a serious prothrombotic disorder caused by heparin exposure. The incidence of thrombosis in patients with isolated HIT, defined as HIT without clinically evident thrombosis at the time of diagnosis, is not well established. Aim: The purpose of this prospective study was to determine the total incidence of thrombotic events after diagnosis of isolated HIT from radiographic evidence of asymptomatic deep venous thrombosis (DVT) plus radiographic confirmation of symptomatic thrombosis. Patients and Methods: We evaluated all patients with a positive enzyme-linked immunoassay (ELISA) for heparin-platelet factor 4 (PF4) antibody (Ab) daily at Massachusetts General Hospital from 10/10/05 to 5/13/06. Inpatients with (1) a positive PF4 Ab test, (2) thrombocytopenia, as defined by a ≥50% drop from baseline platelet count and/or a fall in platelet count to <150×109/L, in association with heparin exposure, (3) no signs or symptoms of thrombosis at time of the positive Ab test, and (4) no other definitive etiology of thrombocytopenia were considered to have isolated HIT and included for study. Patients with a prior diagnosis of HIT, DVT, pulmonary embolism, or peripheral arterial thrombosis were excluded. Within 72 hours of diagnosis and of initiation of a non-heparin anticoagulant, all included patients underwent radiographic examination for asymptomatic DVT in the lower extremities (LE). Objective evidence of thrombotic events other than LE DVT after the diagnosis was also recorded. Daily platelet count, type and timing of all anticoagulants, use of blood products, and PF4 Ab titer were collected to determine if there was an association between these factors and development of thrombosis. Mortality rate during hospitalization was also recorded. Results: Of the 158 patients with a positive heparin-PF4 Ab, 64 patients met criteria for study, 14 of which were lost to follow-up. Among the 50 remaining eligible patients, the total incidence of thrombosis was 20% (12% were found to have an asymptomatic thrombotic event and 8% developed a symptomatic thrombotic event). Development of thrombosis was independently associated with platelet transfusion (p=0.005) and with the degree of platelet count nadir as expressed by platelet count (p=0.038) or by percent decrease from baseline (p=0.031). There was no association between the PF4 Ab titer or the type and timing of non-heparin anticoagulant and development of thrombosis. The overall mortality rate in patients diagnosed with isolated HIT during hospitalization was 22%. Conclusion: The total incidence of thrombotic events in isolated HIT was 20%, with greater than half of the events being asymptomatic thromboses found only by radiographic examination. This high incidence of asymptomatic LE DVT suggests that routine investigation for LE DVT should be performed in this patient population and that patients with isolated HIT should be treated with a non-heparin anticoagulant. Our findings also confirm the current recommendation to avoid platelet transfusions in patients with isolated HIT as we found an increased rate of thrombosis associated with this practice.

scholarly journals Heparin-induced thrombocytopenia (HIT) as an unusual cause of acute stent thrombosis

2009 ◽  
Vol 31 (5) ◽  
pp. 613-613 ◽  
Author(s):  
Rasha K. Al-Lamee ◽  
Robert T. Gerber ◽  
Jaspal S. Kooner
Keyword(s):  
Stent Thrombosis ◽  
Heparin Induced Thrombocytopenia ◽  
Acute Stent Thrombosis

Rapid and simple IgG specific test for the exclusion of heparin induced thrombocytopenia (HIT)

2011 ◽  
Vol 49 (12) ◽  
Author(s):  
Hans-Jürgen Kolde ◽  
Ralf Dostatni ◽  
Susanne Mauracher
Keyword(s):  
Anticoagulation Therapy ◽  
Clinical Samples ◽  
Functional Assay ◽  
Specific Test ◽  
Platelet Factor ◽  
Heparin Induced Thrombocytopenia ◽  
Activation Assay ◽  
Specific Igg ◽  
Positive Results ◽  
Specific Igg Antibodies

AbstractThe exclusion of heparin induced thrombocytopenia (HIT) is required for selecting the most appropriate anticoagulation therapy in affected patients. It requires the combination of clinical data with the detection of antibodies directed against platelet factor 4 (PF4) in complex with polyanions (PA) such as heparin.We developed a lateral flow immunoassay (LFIA) for PF4/PA complex specific IgG antibodies based on gold nanoparticles. Unlike most other assays, the initial immune reaction takes place in the liquid phase. The sensitivity of the assay has been adjusted with clinical samples aiming in the reliable detection of sera which are positive in a functional platelet activation assay.Sera from 60 patients with suspected HIT were investigated. LFIA identified correctly all samples (n=20) which were positive in a functional assay (HIPA) and an IgG specific ELISA. It correlated with ELISA, but false positive results were less frequent (7 samples were negative with LFIA and HIPA but positive with ELISA).The LFIA may be a suitable tool for the rapid exclusion of HIT within 10 min.

Does the Platelet Factor 4 (PF4) ELISA Correlate with the Clinical Diagnosis of Type II Heparin-Induced Thrombocytopenia?.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 2179-2179
Author(s):  
Michael B. Streiff ◽  
Thomas S. Kickler ◽  
Edward G. Weir
Keyword(s):  
Clinical Judgment ◽  
Thrombotic Event ◽  
Anticoagulation Therapy ◽  
Serotonin Release ◽  
Admission Diagnosis ◽  
Type Ii ◽  
Patient Age ◽  
Platelet Factor ◽  
Heparin Induced Thrombocytopenia ◽  
Patient Âgé

Type II heparin-induced thrombocytopenia (HIT) is an antibody-mediated complication of heparin therapy that is associated with a consumptive thrombocytopenia and a high risk of thromboembolism. It is now known that antibodies associated with type II HIT recognize sites on PF4 when complexed with heparin. Due to technical challenges associated with the serotonin release assay, most clinicians rely on the PF4 ELISA to establish a laboratory diagnosis of HIT. However, it is unclear whether the ELISA has predictive value in identifying those patients who have clinically apparent disease and whether ELISA optical density (OD) measurements correlate with the development of thrombosis. We retrospectively reviewed the medical records of 103 sequential patients who tested positive for HIT by a commercial PF4 ELISA from 2000–2002. While blinded to ELISA OD values, we recorded patient age and gender, admission diagnosis, hospital course, type of heparin administered, route of administration, baseline and nadir platelet counts, timing of thrombocytopenia, HIT therapy, clinical thrombotic events within 30 days, and other potential causes of thrombocytopenia to determine the clinical likelihood of HIT. The association between OD values and both the clinical likelihood of HIT and objectively confirmed thrombotic events was analyzed using the Pearson Chi-square test. Median patient age was 62 yrs and 52% of patients were female. Those with cardiac disease, cancer, and venous thromboembolism constituted 44%, 19% and 9% of the study population, respectively. Median platelet count nadir was 40K/mL (range, 2K–90K), and average onset of thrombocytopenia was 6.5 days. Median ELISA OD value was 0.77 (0.40–3.81). The clinical likelihood of HIT was noted in 24/103(23%) patients, and 22(21%) suffered a thrombotic event. An ELISA OD >1.0 was significantly associated with the clinical likelihood of HIT (p=0.03), though OD values ranged from 0.41 to 3.81 among these patients. Neither an OD threshold of 1.0 or 1.5 was associated with thromboembolism (p=0.2 and p=0.1, respectively). In contrast, the clinical likelihood of HIT was significantly associated with subsequent thrombosis (p=0.002). ELISA results were not significantly associated with the extent or onset of thrombocytopenia, type of heparin or route administered, patient age or gender, admission diagnosis, or hospital course. In conclusion, PF4 ELISA OD values are significantly associated with the clinical likelihood of HIT but are not predictive of HIT on an individual patient basis. Clinical judgment but not ELISA OD values is associated with subsequent thromboembolism. In summary, the clinical likelihood of HIT, and not ELISA results, remains the best parameter by which to modify anticoagulation therapy in patients being assessed for HIT. Figure Figure

Comparison of Antigen and Activation Assays with a Probability Scoring Model for the Diagnosis of Heparin Induced Thrombocytopenia.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 3215-3215
Author(s):  
Dimitrios Scarvelis ◽  
Gail Rock
Keyword(s):  
Laboratory Testing ◽  
Laboratory Tests ◽  
Serotonin Release ◽  
Reference Standard ◽  
Platelet Response ◽  
Platelet Factor ◽  
Platelet Recovery ◽  
Heparin Induced Thrombocytopenia ◽  
Activation Assay ◽  
Heparin Anticoagulation

Background: Heparin induced thrombocytopenia (HIT) is a syndrome characterized by thrombocytopenia and an elevated risk of thrombosis. In the evaluation of patients with suspected HIT, laboratory testing is used to help differentiate between those patients who have HIT and those who do not and therefore do not require non-heparin anticoagulation. Laboratory tests include activation (serotonin release, heparin-induced platelet aggregation, ATP luminescence) and antigen (enzyme-linked immunoabsorbant assay (ELISA)) assays directed against the platelet factor 4-heparin or PF4/PVS complex. A pre-test scoring system (Warkentin 4T’s) has been derived to assess the probability of HIT which can be used in conjunction with laboratory testing in the evaluation for HIT. Objectives: To compare the activation assay used at The Ottawa Hospital (ATP luminescence) with the PF4 enhanced® ELISA and correlate results with clinical data. Methods: Patients undergoing HIT testing were identified. ELISA and activation assays were performed. Charts were reviewed in order to derive a 4T’s score and to assess response to therapeutic non-heparin anticoagulation (when administered). Correlation between ELISA, activation assay, 4T’s score and platelet response to alternative anticoagulation was determined. Sensitivity, specificity, PPV and NPV of laboratory tests or 4T’s scores were calculated depending on the measure chosen as the reference standard to diagnose HIT. Results: 111 patients undergoing HIT testing were evaluated. 41 and 43 were positive by ELISA (OD > 0.4) or activation assay respectively. 12 were positive only by ELISA (mean optical density (OD): 1.27) and 10 were positive by both activation assay and ELISA (mean OD: 2.28). Clinical information was available for 70 patients. 26 of these received therapeutic non-heparin anticoagulation as treatment for suspected HIT. Reference standard= activation assay: ELISA: Sens 95% (95% CI 73–99%), Spec 80% (66–89%), PPV 66% (46–81%), NPV 98% (86–100%). 4T’s (low vs. high score): Sens 85% (54–97%), Spec 95% (83–99%), PPV 85% (54–97%), NPV 95% (83–99%). ELISA OD > 1.5 + high 4T’s score: Sens 61% (36–82%), Spec 100% (56–100%), PPV 100% (68–100%), NPV 50% (24–76%). Reference standard= 4T’s score (high and low score only, excludes intermediate category): ELISA: Sens 85% (53–97%), Spec 77% (61–88%), PPV 52% (30–74%), NPV 94% (79–99%). Activation: Sens 85% (54–97%), Spec 95% (83–99%), PPV 85% (54–97%), NPV 95% (83–99%). Reference standard= “clear response to non-heparin anticoagulation” defined as significant platelet increase within 48 hours of start of therapy and no other explanation for platelet recovery: ELISA: Sens 100% (72–100%), Spec 54% (26–80%), PPV 68% (43–86%), NPV 100% (56–100%). Activation: Sens 85% (54–97%), Spec 69% (39–90%), PPV 73% (45–91%), NPV 82% (48–97%). 4T’s (low vs. high score): Sens 90% (54–99%), Spec 100% (60–100%), PPV 100% (63–100%), NPV 89% (51–99%). ELISA OD > 1.5 + 4T’s (low vs. high score): Sens 89% (51–99%), Spec 100% (56–100%), PPV 100% (60–100%), NPV 88% (47–99%). Conclusions: A high 4T’s score best predicts a clinical response to non-heparin therapeutic anticoagulation when HIT is suspected. ELISA OD > 1.5 does not add additional information in this respect. A negative ELISA and a low 4T’s score have comparable NPVs when an activation assay is the reference standard. Future trials should employ a clinical reference standard such as “clear response to non-heparin anticoagulation” when evaluating the operator characteristics of HIT assays.

Spontaneous Heparin-Induced Thrombocytopenia Syndrome: Two New Cases and a Proposal For Defining This Disorder

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 2328-2328 ◽  
Author(s):  
Theodore E. Warkentin ◽  
Paul Andrew Basciano ◽  
Richard A. Bernstein
Keyword(s):  
Platelet Count ◽  
Platelet Activation ◽  
Research Funding ◽  
Left Vertebral Artery ◽  
Platelet Factor ◽  
Shoulder Hemiarthroplasty ◽  
Heparin Induced Thrombocytopenia ◽  
Activation Assay ◽  
Count Recovery ◽  
Heparin Exposure

Abstract Introduction Heparin-induced thrombocytopenia (HIT) is a transient, autoimmune-like, prothrombotic disorder caused by heparin-dependent, platelet-activating IgG reactive against platelet factor 4/heparin (PF4/H). There is an emerging literature (Am J Med 2008;121:632-6. J Thromb Haemost 2008;6:1598-1600; Thromb Haemost 2013;109:669-75) pointing to rare instances of “spontaneous” HIT in patients without preceding heparin. We report 2 new cases and propose a definition for this controversial disorder. CASE #1. A 62-y.o. man presented with left middle cerebral artery stroke and thrombocytopenia (platelet count, 65×109/L). There was no previous history of thrombocytopenia, surgery, hospitalization, or heparin exposure. Clot extraction performed with heparin was complicated by further platelet count decline to 27 (nadir) and progressive thrombosis of the carotid artery. Aspirin was started, and the platelets recovered to >150 by day 13. CASE #2. A 54-y.o. female developed right leg swelling, left-upper extremity weakness/paresthesias, and thrombocytopenia (61×109/L) 15 days post-shoulder hemiarthroplasty; no intra-/postoperative heparin had been given. Brain MRI demonstrated acute infarct in the left posterior inferior cerebellar artery territory; angiography showed non-visualization of the left vertebral artery. Ultrasound revealed right lower-limb deep-vein thrombosis. Heparin treatment resulted in further platelet count fall to 37 (nadir). Treatment with argatroban, followed by fondaparinux, was associated with platelet count recovery to >150 by day 39. Methods Testing for HIT antibodies was performed by commercial EIA-IgG/A/M (Immucor GTI Diagnostics), in-house EIA-IgG (McMaster), and serotonin-release assay (SRA). Results Both patients’ sera (obtained before any heparin administration) tested strongly positive for HIT antibodies (Table), including strong platelet activation at 0.1 and 0.3 IU/mL heparin, as well as at 0 U/mL heparin, with no platelet activation at 100 IU/mL heparin: these serological features are characteristic of “delayed-onset HIT” (Ann Intern Med 2001;135:502-6). Antibody reactivity declined markedly by 2 to 4 weeks (including loss of platelet-activating properties at 0 IU/mL heparin), in keeping with the usual transience of HIT antibodies (N Engl J Med 2001;344:1286-92), and paralleling both patients’ platelet count recovery. Discussion These cases further support spontaneous HIT as an unusual explanation for acute arterial stroke and thrombocytopenia. One patient had preceding orthopedic surgery, an event previously reported with spontaneous HIT (Thromb Haemost 2013;109:669-75). The strong serum-dependent platelet activation at 0 IU/mL heparin helps to explain how thrombocytopenia and thrombosis can occur in a patient not receiving heparin. RECOMMENDATION. Based on the serological findings of these and previous cases, we propose that a definitive diagnosis of spontaneous HIT syndrome should be based upon all of the following criteria: thrombocytopenia, thrombosis, lack of proximate heparin exposure, strong-positive PF4-dependent immunoassay(s), and a strong-positive platelet activation assay featuring both heparin-dependent (e.g., high heparin neutralization) and heparin-independent platelet activation (at 0 IU/mL heparin). Disclosures: Warkentin: Pfizer Canada: Honoraria; Paringenix: Consultancy; Immucor GTI Diagnostics: Research Funding; WL Gore: Consultancy; GSK: Research Funding.

scholarly journals Acute Stent Thrombosis and Heparin Induced Thrombocytopenia: Another Manifestation of Kounis Syndrome?

2013 ◽  
Vol 43 (4) ◽  
pp. 221
Author(s):  
Nicholas G Kounis ◽  
George D Soufras ◽  
George Almpanis ◽  
Grigorios Tsigkas ◽  
Andreas Mazarakis
Keyword(s):  
Stent Thrombosis ◽  
Kounis Syndrome ◽  
Heparin Induced Thrombocytopenia ◽  
Acute Stent Thrombosis
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